Concurrent infection with Schistosoma mansoni attenuates inflammation induced changes in colonic morphology, cytokine levels, and smooth muscle contractility of trinitrobenzene sulphonic acid induced colitis in rats
- T G Moreels1,
- R J Nieuwendijk1,
- J G De Man1,
- B Y De Winter1,
- A G Herman3,
- E A Van Marck2,
- P A Pelckmans1
- 1Division of Gastroenterology, Faculty of Medicine, University of Antwerp (UA), Universiteitsplein 1, B-2610 Wilrijk, Belgium
- 2Division of Pathology, Faculty of Medicine, University of Antwerp (UA), Universiteitsplein 1, B-2610 Wilrijk, Belgium
- 3Division of Pharmacology, Faculty of Medicine, University of Antwerp (UA), Universiteitsplein 1, B-2610 Wilrijk, Belgium
- Correspondence to:
Professor P A Pelckmans
Faculty of Medicine-Division of Gastroenterology, University of Antwerp, Universiteitsplein 1, B-2610 Wilrijk, Belgium;
- Accepted 26 August 2003
Background and aims: Crohn’s disease, characterised by chronic T helper 1 (Th1) inflammation and dysmotility of the gut, is most prevalent in developed countries. Parasitic infections are most prevalent in developing countries and induce a T helper 2 (Th2) immune response. We hypothesised that this Th2 immune response protects against Th1 gut inflammation.
Methods: The parasite Schistosoma mansoni induces a transient Th2 immune response in the semipermissive rat host. 2,4,6-Trinitrobenzene sulphonic acid (TNBS) induced colitis is an experimental model of Th1-like gut inflammation. The effect of concurrent infection with S mansoni on the course of TNBS induced colitis was assessed using macroscopic and microscopic damage scores, histology, myeloperoxidase (MPO) activity assay, cytokine production assay, and by studying in vitro contractility of longitudinal and circular colonic muscle strips.
Results: TNBS induced colitis that spontaneously healed after four weeks. Concurrent infection with S mansoni significantly reduced the duration of TNBS induced colitis to two weeks, as shown by macroscopic and microscopic damage scores and by a faster decrease in colonic MPO activity. TNBS increased colonic interleukin 2 (IL-2) production whereas S mansoni increased splenic IL-4 and IL-2 levels. Contractility of longitudinal and circular muscle strips was maximally inhibited one week after TNBS and normalised after three weeks. After four weeks, longitudinal muscle strip contractility was significantly increased. Concurrent infection with S mansoni normalised longitudinal muscle contractility after one week whereas circular muscle contractility remained inhibited.
Conclusions: Concurrent infection with S mansoni significantly attenuates TNBS induced colitis in the rat. Inflammation induced disturbances in contractility of longitudinal and circular colonic muscle strips may outlast the inflammatory reaction.
- ACh, acetylcholine
- Emax, maximal contractile response
- CSA, cross sectional area
- IFN-γ, interferon γ
- IL, interleukin
- MPO, myeloperoxidase
- Th, T helper
- TNBS, 2,4,6-trinitrobenzene sulphonic acid